Signal transducer and activator of transcription 3 (STAT3), a member of the STAT family, is a transcription factor that plays a key role in cell proliferation and differentiation. STAT3 dimerizes upon phosphorylation and migrates into nucleus to activate the transcription of cytokine-responsive genes. In physiological conditions, the expression and activation of STAT3 are finely regulated by multiple mechanisms. Aberrant regulation of the STAT3 signaling pathway has been frequently observed in several malignancies.
A complete picture of the mechanisms by which STAT3 signaling pathway is dysregulated in cancer is still missing. Due to its prominent role in both solid tumors and hematological malignancies, further studies are critical to better understand the role of STAT3 in tumor progression and possible strategies to counteract it.
This Research Topic will focus on the description of mechanisms through which the upregulation of STAT3 signaling contributes to cancer progression, such as in glioblastoma, neuroblastoma, breast, lung and other cancers. We are particularly interested in studies related to endogenous tumor suppressors and/or microRNAs that block STAT3 activity at both the cytoplasmic and/or nuclear levels. Accordingly, the counteractive effect would lead to suppression of cancer growth.
We welcome the submission of Original Research and Review articles that cover, but are not limited, to the following topics:
• Mechanisms of regulation of STAT3 pathway
• Effectors of STAT3 regulatory signaling network
• Endogenous or exogenous nuclear inhibitors for STAT3
• New emerging roles for STAT3 in aberrant signaling during cancer development
• Synthetic STAT3 signaling inhibitors and their mechanisms of action
• Combination of STAT3 inhibitors and other treatment modalities for cancer therapy
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Signal transducer and activator of transcription 3 (STAT3), a member of the STAT family, is a transcription factor that plays a key role in cell proliferation and differentiation. STAT3 dimerizes upon phosphorylation and migrates into nucleus to activate the transcription of cytokine-responsive genes. In physiological conditions, the expression and activation of STAT3 are finely regulated by multiple mechanisms. Aberrant regulation of the STAT3 signaling pathway has been frequently observed in several malignancies.
A complete picture of the mechanisms by which STAT3 signaling pathway is dysregulated in cancer is still missing. Due to its prominent role in both solid tumors and hematological malignancies, further studies are critical to better understand the role of STAT3 in tumor progression and possible strategies to counteract it.
This Research Topic will focus on the description of mechanisms through which the upregulation of STAT3 signaling contributes to cancer progression, such as in glioblastoma, neuroblastoma, breast, lung and other cancers. We are particularly interested in studies related to endogenous tumor suppressors and/or microRNAs that block STAT3 activity at both the cytoplasmic and/or nuclear levels. Accordingly, the counteractive effect would lead to suppression of cancer growth.
We welcome the submission of Original Research and Review articles that cover, but are not limited, to the following topics:
• Mechanisms of regulation of STAT3 pathway
• Effectors of STAT3 regulatory signaling network
• Endogenous or exogenous nuclear inhibitors for STAT3
• New emerging roles for STAT3 in aberrant signaling during cancer development
• Synthetic STAT3 signaling inhibitors and their mechanisms of action
• Combination of STAT3 inhibitors and other treatment modalities for cancer therapy
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.